8 Amino Acids for ADHD

In a review of natural product-derived treatments for ADHD, Ahn et al. (2016) explain how the amino acids glycine, L-theanine, L-tyrosine, taurine, acetyl-L-carnitine (ALC), GABA, 5-hydroxytryptophan (5-HTP), are all considered potential complementary ADHD interventions.  The authors’ review was thorough, but since we don’t take anything at face value, let’s take a deeper look at each one of these amino acids, how they might help, and studies that have demonstrated their efficacy.

As I have mentioned in my previous posts, each individual with ADHD is unique.  This means that what works for one may not work for all, because individual causes for ADHD will vary. You know your child best, and you know yourself best. That being said, considering the dangers of stimulant medications, I believe natural therapies are certainly worth trying under the supervision of your health care provider.  Consistency is key. Some may experience immediate results, but some may need to be consistent and give the body time to adjust. Let us begin.

L-Glycine

Glycine is an inhibitory (calming) neurotransmitter and it plays a role in regulating the motor and sensory information that permits movement, vision, and hearing.  It modulates excitatory neurotransmission by increasing the effect of glutamate (the most abundant neurotransmitter in the brain) and also plays a role in transporting GABA (our primary inhibitory neurotransmitter) between neurons.  In essence, L-Glycine is essential for proper brain balance of GABA and glutamate. A disruption of this balance has been implicated as a potential cause for ADHD, and drugs that promote that balance are being researched (Malapati et al., 2015). In fact, stimulant medications greatly increase the amount of glutamate in the brains of healthy people, and may be part of the reason that they work for children with ADHD (Brown University, 2018).  It is logical to supplement with a calming amino acid that supports this balance.

Glycine is one of the three amino acid precursors of the most powerful antioxidant  glutathione (produced by the liver).  According to Aksoy et al. (2016),  there is significantly increased oxidative stress in children with ADHD.  Supporting their ability to combat that oxidative stress by supplying adequate glutathione precursors is essential.  The other two glutathione precursors are L-cysteine and L-glutamate.

“Balance between excitatory glutamate and inhibitory GABA neurotransmitter is essential and critical for proper development and functioning of brain.” – Current Medicinal Chemistry, Malapati et al., 2015

I know you may want to rush out and buy some glutathione, but the body does not utilize glutathione well if taken directly.  It is better to support the body’s ability to synthesis it.  NAC (N-acetyl-cysteine) is another powerful supplement that supports glutathione production in the liver.  I will be posting more about glutathione in the future.

GABA Precursors

GABA is an amino acid and a neurotransmitter that has a calming effect on the brain.  Crocetti et al (2012) studied brain scans and found children with ADHD have reduced concentrations of GABA. So why not take GABA?  It appears GABA supplements do not cross the blood brain barrier very effectively in ADHD.  It is better to take the GABA precursors L-Theanine, L-Glutamine, and Vitamin B6 in its activated form P5P.  Taking the precursors gives the brain what it needs to make adequate GABA.  

L-Theanine

One study in which boys age 8 to 12 years old were given 400mg L-theanine daily demonstrated that L-Theanine may represent a safe and important adjunctive therapy in ADHD (Juneja et al, 2011).  Theanine is able to cross the blood brain barrier and has been proven to alleviate symptoms of anxiety and improve ADHD symptoms by helping to regulate dopamine and serotonin as well as increase the production of inhibitory (calming) neurotransmitters (Lardner, 2014; Ahn et al., 2016).  L-Theanine has been proven to improve cognitive function including learning, attention, and memory (Lardner, 2014).

L-Tryptophan

One theory for the cause of ADHD is rather than an issue with the quantity of available dopamine and norepinephrine, there is some kind of disturbance in the blood brain barrier that does not allow enough of the amino acid tryptophan to be transported across it (Ahlin et al., 2011).  Tryptophan deficiency within the brain would not necessarily appear in typical blood work.  To clarify, a person may have plenty of tryptophan circulating in their blood, but if the blood brain barrier won’t let enough of it in, there is a brain deficiency (and there is not currently an easy, available, and safe way to study brain deficiencies).  And if there is a brain deficiency of tryptophan it can be assumed that there is also a serotonin deficiency since the brain utilizes tryptophan to create serotonin. This would disturb the serotonin-dopamine balance, which plays a role in ADHD symptoms.

It seems reasonable that supplementing with L-tryptophan would increase the available circulating tryptophan, and potentially allow more of it to cross the blood brain barrier.

To read more on L-Tryptophan and the serotonin-dopamine balance in ADHD read my previous post L-Tryptophan for ADHD: Amino Acids Reduce Symptoms

OR this maple flavored chewable version:

Taurine

Taurine is an amino acid made in the liver from cysteine that is known to play a role in the brain by eliciting a calming effect.” Lakhan & Vieira, Nutrition Journal, 2008

In an animal study, taurine reduced hyperactivity symptoms so significantly that it was proposed as an alternative treatment for ADHD (Chen et al., 2017).

Ripps and Shen (2012) emphasize the importance of taurine in their article “Review: Taurine: A “very essential” amino acid.”  The authors explain that taurine is vital for normal brain development, for the protection of neurons and cells from toxic agents, for modulation of brain activity, and for modulation of intracellular calcium (Ripps & Shen, 2012).  It also meets many criteria for consideration as a neurotransmitter, although a specific receptor site for taurine has yet to be found (Ripps & Shen, 2012). Kim and Schaffer (2018) further confirm the importance of taurine in their article “Effects and Mechanisms of Taurine as a Therapeutic Agent.”  They explain that taurine is anti-inflammatory, antioxidant, lowers cholesterol, helps to treat cardiovascular disease and high blood pressure, regulates energy metabolism, regulates gene expression, and even inhibits brain injury in stroke and Alzheimer’s disease (Kim & Schaffer, 2018). I was unable to find any studies that specifically focused on taurine for ADHD, however studies and reviews do demonstrate that it is a GABA and L-glycine agonist (we have already discussed the research on GABA and L-Glycine for ADHD above).  It is clearly vital for brain and overall health. I expect to see research on taurine and ADHD in the future.

Acetyl-L-carnitine (ALC)

ALC and L-Carnitine are used to transport fatty acids into cell mitochondria.  The body can change ALC into L-carnitine as needed, and visa versa (it can also change L-carnitine into ALC).  The importance of essential fatty acids for overall health (especially brain and heart health) has been well established.  Indeed, essential fatty acid (EFA) supplementation is also extremely beneficial for ADHD (stay tuned for future post on EFAs).  Here we are focusing on how ALC helps us properly utilize those healthy fats.

“Treatment with carnitine significantly decreased the attention problems and aggressive behavior in boys with ADHD.” Van Oudheusden & Scholte, PLEFA Journal, 2002

Another study found that in Fragile X Syndrome (FXS) children with ADHD, treatment with ALC at doses of 20-50 mg/kg/day was very effective and considered a safe alternative to the use of stimulant drugs for the treatment of ADHD in FXS children (Calvani et al., 2008).

In a study on boys and girls ages 5 through 12, Amato et al. (2007) found that Acetyl-L-Carnitine supplementation at weight-based doses from 500 to 1500 mg twice per day was more effective for inattentiveness than for hyperactivity.

L-Tyrosine

L-tyrosine increases catecholamine production.  Ahn et al. (2016) explain that ADHD is associated with disruption in catecholaminergic function in the brain.  In fact, stimulant medications seem to mimic catecholamines as well as increase dopamine and norepinephrine levels, which seems to restore catecholamine balance.  The problem is that these medications are dangerous, damage the liver, and damage long term brain health. By contrast, L-tyrosine is an amino acid found in protein-rich foods that we eat every day.  L-tyrosine is the amino acid that is required for the production of dopamine, norepinephrine, and epinephrine. Cofactors include B6 (P5P), vitamin C, iron, and copper.  Check your child’s multivitamin to be sure these cofactors are present, or be sure that your child is eating healthy foods that are rich in these nutrients.  If you are not sure how much B6 is safe for supplementation, here is the chart for established upper intakes according to the National Institutes of Health (2018):

b6 upper intakes

One retrospective study by Hinz et al. (2011) demonstrated that the use of a protocol including L-Tyrosine, 5-HTP and the necessary cofactors resulted in significant improvement of ADHD symptoms in 77% of study participants. They monitored neurotransmitter levels via urine testing during the stages of the study, and concluded that their results were actually superior to that of stimulant medication studies.  Hinz et al. (2011) emphasize:

“Even if the finding was that use of serotonin and dopamine amino acid precursors with OCT assay interpretation was equal to reported efficacy values found with atomoxetine and methylphenidate, it is asserted that this approach would be superior because it does not share the adverse reactions, potential depletion of neurotransmitters, and neurotoxicity concerns reported with the group of drugs prescribed for ADHD treatment.”

5-hydroxytryptophan (5-HTP)

5-HTP is a naturally occurring amino acid derived from the African plant known as Griffonia simplicifolia.  It is able to cross the blood brain barrier, and it is a precursor to serotonin production (keep in mind that our bodies make melatonin from serotonin).  Serotonin also plays a role in regulating dopamine. Kennealy, Patrick, and Seo (2008) explain that serotonin deficit could lead to symptoms of dopamine excess, and visa versa.

Dr. Hinz and his colleagues propose that an imbalance between serotonin and dopamine is the cause for a variety of disorders, including ADHD.  They use urine testing to guide amino acid therapy and to evaluate if their amino acid protocol achieves the intended balance. As I mentioned above, the study demonstrates that balancing these neurotransmitters appears to significantly reduce or eliminate ADHD symptoms.  I strongly recommend that you work with your health care provider if you want to try the L-tyrosine/5-HTP amino acid therapy.  For information purposes, here is the Hinz protocol according to the 2011 study (link found in references).  Patients start with level one, if symptoms are relieved they do not advance to level 2.  If symptoms persist on level one dosing, the patient is advanced to level two dosing. If symptoms resolve, they do not advance.  You get the idea. If symptoms persist even after level three dosing, the patient is reevaluated. Important to mention is that supplementing with only one of these may result in further imbalance.

hinz protocol

OR this sweet tasting lozenge version:

If you have any questions or comments, or if you feel it is necessary to correct something that you read here, feel free to do so below. I appreciate any and all of your contributions. If you think this post could help a friend, share it. You just might change their life.

Related Posts

Top 6 ADHD Triggers To Nix: Stop Giving THESE to Your Child

L-Tryptophan for ADHD: Amino Acids Reduce Symptoms

Long Term Effects of ADHD Stimulant Medications

Legal Disclaimer: The information, including but not limited to, text, graphics, images, website links and other material contained on this website are for informational purposes only. The purpose of this website is to promote broad consumer understanding and knowledge of various health topics, as well as share personal opinions and experiences. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified healthcare provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this website.

References

Ahlin, A., Bejerkenstedt, L., Fernell, E., … (2011). Altered tryptophan and alanine transport in fibroblasts from boys with attention-deficit/hyperactivity disorder (ADHD): an in vitro study. Retrieved from https://behavioralandbrainfunctions.biomedcentral.com/articles/10.1186/1744-9081-7-40

Ahn, H., Ahn, J., Cheong, J., & Pena, I. (2016). Natural Product-Derived Treatments for Attention-Deficit/Hyperactivity Disorder: Safety, Efficacy, and Therapeutic Potential of Combination Therapy. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757677/

Aksoy, N., Basmaci Kandemir, S., Bilinc, H., Kandemir, H., Kilicaslan, F., Savik, E., & Sezen, H. (2016). Increased oxidative stress in children with attention deficit hyperactivity disorder. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/26886057

Amato, A., Arnold, L., Bozzolo, H., Cook, A., Crowl, L., Hollway, J., . . . Zhang, D. (2007). Acetyl-L-carnitine (ALC) in attention-deficit/hyperactivity disorder: a multi-site, placebo-controlled pilot trial. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/18315451

Brown University. (2018). ADHD drugs increase brain glutamate, predict positive emotion in healthy people. Retrieved from https://news.brown.edu/articles/2018/03/glutamate

Calvani, M., Chiurazzi, P., Cocchi, E., D’Iddio, S., Frontera, M., Garbarino, E., . . . & Vernacotola, S. (2008). A double-blind, parallel, multicenter comparison of L-acetylcarnitine with placebo on the attention deficit hyperactivity disorder in fragile X syndrome boys. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/18286595

Chen, L., Chen, V., Chou, H., Hsu, T., Tzang, B., & Weng, J. (2017). Effects of taurine on resting-state fMRI activity in spontaneously hypertensive rats. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5507323/

Crocetti, D., Edden, R., Gilbert, D., Mostofski, S., & Zhu, H. (2012). Reduced GABA concentration in Attention-Deficit/Hyperactivity Disorder. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3970207/

Hinz, M., Neff, R., Stein, A., Uncini, T., & Weinberg, R. (2011). Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035600/

Juneja, L., Kapoor, M., & Lyon, M. (2011). The effects of L-theanine (Suntheanine) on objective sleep quality in boys with Attention Deficit Hyperactivity Disorder (ADHD): a randomized, double-blind, placebo-controlled clinical trial. Retrieved from http://archive.foundationalmedicinereview.com/publications/16/4/348.pdf

Kennealy, P., Patrick, C., & Seo, D. (2008). Role of Serotonin and Dopamine System Interactions in the Neurobiology of Impulsive Aggression and its Comorbidity with other Clinical Disorders.  Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2612120/

Kim, H. & Schaffer, S. (2018). Effects and Mechanisms of Taurine as a Therapeutic Agent. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933890/

Lakhan, S. & Vieira, K. (2008). Nutritional therapies for mental disorders. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2248201/

Lardner, A. (2014). Neurobiological effects of the green tea constituent theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23883567/

Malapati, A., Purkayastha, P., Sriram, D., & Yogeeswari P. (2015). A Review on GABA/Glutamate Pathway for Therapeutic Intervention of ASD and ADHD. Retrieved from  https://www.ncbi.nlm.nih.gov/pubmed/25666800

Ripps, H. & Shen, W. (2012). Review: Taurine: A “very essential” amino acid. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501277/

Van Oudheusden, L. & Scholte, H. (2002). Efficacy of carnitine in the treatment of children with attention-deficit hyperactivity disorder. Retrieved from https://www.plefa.com/article/S0952-3278(02)90378-9/pdf

Top 6 ADHD Triggers To Nix: Stop Giving THESE to Your Child

1. Artificial Food Coloring: Lay off the Fruit Loops

Artificial Food Coloring that is found in many foods marketed to children and adolescents are known to contribute significantly to ADHD and in some cases may push a child over the diagnostic threshold (Arnold, 2012). Artificial food coloring has been proven to interfere significantly with the absorption of zinc, which is essential for normal brain function. According to Aizenman et al. (2011), zinc is “intimately linked to the balance excitation and inhibition in the brain.” Given this, it is reasonable to assume that eliminating food coloring may reduce your child’s ADHD symptoms so significantly that they will no longer qualify for the diagnosis of ADHD.

2. Screen Time: Get Their Face Off The Phone/Tablet

A recent study found that there was a significant association between higher frequency of digital media use and subsequent symptoms of ADHD over a two year follow-up (Cho, Stone, & Ra, 2018). This research poses the question: could the use of digital media such as video games or even “educational” games on a tablet lead to the development of ADHD? It seems obvious that if screen time can potentially cause ADHD symptoms, it would make symptoms worse when ADHD already exists. More research is needed, but the association is clear.

3. Video Games: Winning at a Cost

Video are known to reduce the number of dopamine receptors and transporters, change brain function, create abnormalities in gray and white brain matter, and cause decreased neural connectivity (Sigman, 2014).. Remember, video games are not just the ones with remote controls. The games children and adolescents play on their tablets and phones (yes, even if they are deemed educational) are still video games. All the distractions online make it even more difficult for people with ADHD to focus (Understood.org, 2018).

4. Sodas: Kick the Coke

Soft drinks contain a preservative called sodium benzoate. A scientific literature review asserted that sodium benzoate intake contributes significantly to ADHD symptoms (Anjum et al., 2018). Ingestion of sodium benzoate leads to a rise in anthranilic acid and acetylglycine (Clish, et al., 2014). Anthranilic acid is involved in tryptophan metabolism in both humans and bacteria, and therefore it likely has a negative impact on tryptophan metabolism. In some studies tryptophan supplementation has been shown to reduce ADHD symptoms, so it seems logical to avoid anything that might disrupt its utilization. Anthranilic acid is also found in corn, and corn is everywhere. Sodium benzoate has many other adverse health effects worth knowing about since it exists in so many foods.

5. Sedentary Lifestyle: Get off Your . . .

I’m sure you have read that exercise helps ADHD somewhere. I have ready many lists that include exercise but none of them explain why exercise helps ADHD. Regular physical exercise is especially beneficial for children with ADHD, because cardio exercise increases specific catecholamines and proteins/enzymes that are typically reduced in ADHD such as dopamine, tyrosine hydroxylase and brain-derived neurotrophic factor (Fuermaier et al., 2016). “Existing studies reveal that high levels of sedentary behavior are associated with more inattention and hyperactivity problems” (Hanewinkel et al., 2017). So do yourself and your children a favor and get off your . . .

6. Inflammatory Foods: Flames from French Fries?

Simple sugars, a high carbohydrate diet, and foods high in omega 6 are inflammatory. Canola oil, corn oil, soybean oil, and other vegetable fats are inflammatory because the body metabolizes them into arachidonic acid. We only use ghee, olive oil, or coconut oil in our home. Drisko et al (2014) assert that many children and teens with ADHD have high levels of inflammatory markers, potentially due to imbalance of omega-3 and omega-6 fats and not enough polyunsaturated fatty acids. Avoiding inflammatory foods and eating anti-inflammatory healthy foods and fats is integral to our health. Warning: Most store bought mayonnaise and salad dressings are made with canola or soybean oil, and those same inflammatory oils are used to make fried foods. Check your labels!

If you have any questions or comments, or if you feel it is necessary to correct something that you read here, feel free to do so below. I appreciate any and all of your contributions. If you think this post could help a friend, share it. You just might change their life.

Related posts

Long Term Effects of ADHD Stimulant Medications

L-Tryptophan for ADHD: Amino Acids Reduce Symptoms

Legal Disclaimer: The information, including but not limited to, text, graphics, images, website links and other material contained on this website are for informational purposes only. The purpose of this website is to promote broad consumer understanding and knowledge of various health topics, as well as share personal opinions and experiences. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified healthcare provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this website.

References

Aizenman, E., Bush, A., Paoletti, P., Hershfinkel, M., Koh, J., & Sensi, S. (2011). The neurophysiology and pathology of brain zinc. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3223736/

Anjum, I., Armghan, H., Fayyaz, M., Jaffery, S., & Wajid, A. (2018). Sugar beverages and dietary sodas impact on brain health: A mini literature review. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6080735/

Arnold, L., Hurt, E., & Lofthouse, N. (2012). Artificial food colors and attention-deficit/hyperactivity symptoms: Conclusions to dye for. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3441937/

Cho, J., Stone, M., & Ra, C. (2018). Association of digital media use with subsequent symptoms of attention-deficit/hyperactivity disorder among adolescents. Retrieved from https://jamanetwork.com/journals/jama/article-abstract/2687861

Clish, C., Deik, A., Delaney, N., Lennerz, B., Ludwig, D., Mootha, V., Pierce, K., & Vafai, S. (2014). Effects of sodium benzoate, a widely used food preservative, on glucose homeostasis and metabolic profiles in humans. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289147/

Drisko, J., Esparham, A., Evans, R., & Wagner, L. (2014). Pediatric Integrative Medicine Approaches to Attention Deficit Hyperactivity Disorder (ADHD). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4928725/

Fuermaier, A., Groen, Y., Den Heijer, A., Lange, K., Koerts, J., Thome, J., & Tucha, O. (2016). Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: a systematic literature review. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5281644/

Hanewinkel R., Pedersen, A., Isensee, B., & Suchert, V. (2017). Relationship between attention-deficit/hyperactivity disorder and sedentary behavior in adolescence: a cross-sectional study. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28378132

Sigman, A. (2014). Virtually addicted: why general practice must now confront screen dependency. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4240116/

L-Tryptophan for ADHD: Amino Acids Reduce Symptoms

Attention Deficit Hyperactivity Disorder (ADHD) is considered a neurodevelopmental disorder. Currently, the treatment for this disorder is primarily with various forms of the central nervous system stimulants methylphenidate and amphetamine. There is very little research on the long term effects of these drugs, and what we know from the research that does exist is not encouraging.

For instance, we know that long-term use of stimulants, even as prescribed by a physician, can lead to tolerance and the need for higher and more frequent doses to get the desired effect (National Institute on Drug Abuse, 2018).

There are some nonstimulants that were approved for use with children who do not respond well to stimulants (FDA, 2017). The nonstimulants include Strattera (atomoxetine), Intuniv (guanfacine), and Kapvay (clonidine).  These were approved for this use quite recently, so the effects of long term use has yet to be determined (FDA, 2017). Atomoxetine was approved in 2003; Guanfacine was approved in 2009; and Clonidine was approved only in 2010.

Unfortunately, people are needing to choose between the ADHD symptoms and the often equally cumbersome side effects of nonstimulants. The use of nonstimulants is not nearly as common as the use of stimulants, so this post is going to be focusing on stimulant use. The amino acid we will be focusing on here is L-Tryptophan. L-tryptophan is a precursor to serotonin, which means it is nutritionally essential for the production of serotonin.

There are various studies underway which are trying to determine the “cause” of ADHD. I personally don’t believe there is one specific cause for all who are diagnosed with ADHD, and it is also widely accepted that regardless of the diagnosis, there are many factors that may exacerbate ADHD symptoms (diet, environmental exposures, etc). The very fact that stimulants work for many children but not ALL of them is at least one good indicator that the root cause of ADHD may not always be exactly the same from one child to the next. We are all unique individuals, after all.

Okay so you may be asking, “How does a stimulant work to help calm down and focussomeone? A stimulant should stimulate right?.” Well, yes and no.

It should be noted that the mode of action of stimulants in ADHD is not well understood. Just as there are various theories for the cause of ADHD, there are also various theories on how drugs work to affect ADHD. This means that stimulants are given to ADHD patients, and they work, but we don’t exactly know how they work. One theory is that they prevent the reuptake of dopamine and norepinephrine, which increases the activity of those neurotransmitters in a part of the brain called the prefrontal cortex. The prefrontal cortex is responsible for impulse control, decision making, moderating the way we behave in social situations, and complex planning. Another theory that I find interesting is the hypothesis that rather than an issue with the quantity of available dopamine and norepinephrine, there is some kind of disturbance in the blood brain barrier that does not allow enough of the amino acid tryptophan to be transported across it (Ahlin et al., 2011).  Tryptophan deficiency within the brain would not necessarily appear in typical blood work.  To clarify, a person may have plenty of tryptophan circulating in their blood, but if the blood brain barrier won’t let enough of it in, there is a brain deficiency (and there is not really a safe way to study brain deficiencies). And if there is a brain deficiency of tryptophan it can be assumed that there is also a serotonin deficiency since the brain utilizes tryptophan to create serotonin.

Wait, weren’t we talking about dopamine? Yes, indeed we were. Hang with me here. Serotonin and dopamine essentially work together–in a way, they are constantly balancing each other out.

The serotonergic system directly influences the dopamine system, and a chronic deficiency of serotonin at the point where brain neurotransmitters allow communication between two neurons (called a synapse) is known to trigger symptoms of ADHD (Banerjee & Nandagopal, 2015).

So a serotonin deficiency could negatively impact dopamine levels and activity in the brain. This may be why L-tryptophan supplementation significantly alleviates ADHD symptoms (Banerjee & Nandagopal, 2015). To me, it makes sense that increasing the available circulating tryptophan via supplementation or diet would help more of it move across the blood brain barrier.

This is further supported by the prevalence of ADHD among alcoholics, as the consumption of alcohol increases brain concentrations of serotonin (WebMD, 2018).

Perhaps ADHD patients are more prone to alcoholism partly because they are deficient in serotonin.  There is a lot of literature (in books, journals, and online medical resources) that suggests supplementation with tryptophan helps to alleviate the symptoms of ADHD.  I have also read many anecdotal stories from adults diagnosed with ADHD and from parents with children who have ADHD who found that tryptophan or 5HTP supplementation helped tremendously. 5HTP is known to increase serotonin levels and is commonly used in combination with other amino acids for various health issues.

Finally, L-tryptophan may not work for everyone with ADHD.  Remember, each individual in unique.  There are many other alternative approaches, and I encourage you to do your research before any final decisions are made.

If you do decide to give your child a tryptophan supplement (which is found in animal and plant proteins that we eat every day), or if you decide to take it yourself, it should be under the care and supervision of your physician.

There is a brand called Lidtke that makes a chewable tryptophan tablet. I have tasted it, and can tell you that it smells like pancakes and tastes like maple syrup.  In general, it is best to take a pure form of L-tryptophan such as this powder version from NutraBio. Pure L-tryptophan doesn’t taste wonderful, but its not terrible either. It is also available in pill form but I always try to take the powdered form of amino acids because I don’t necessarily want to ingest any unnecessary additives or the capsule itself.  If you are supplementing with L-Tryptophan it is essential to also supplement with Vitamin B6 (as P5P, which is the activated form of B6) because B6 is necessary for L-tryptophan to make its necessary conversions.  Here is a chewable B6 made by EZ Melts, and here is a pill form by Pure Encapsulations.  B6 also supports healthy metabolism of carbohydrates, fats, and proteins.

Another amino acid that may help with ADHD is L-Tyrosine, especially when used in combination with the 5HTP (from the seeds of an African plant known as Griffonia simplicifolia) but that requires a different post for more detailed information (which I will be writing soon enough).  Please subscribe to get notified of new posts.  (To the right on your desktop and at the bottom of the screen on your cell phone).

If you have any questions or comments, or if you feel it is necessary to correct something that you read here, feel free to do so below. I appreciate any and all of your contributions. If you think this post could help a friend, share it. You just might change their life.

Related posts

Long Term Effects of ADHD Stimulant Medications

Top 6 ADHD Triggers To Nix: Stop Giving THESE to Your Child

8 Amino Acids for ADHD

Top 10 Natural Therapies for ADHD (Coming soon)

Cannabidiol (CBD Oil) for ADHD (Coming soon)

Legal Disclaimer: The information, including but not limited to, text, graphics, images, website links and other material contained on this website are for informational purposes only. The purpose of this website is to promote broad consumer understanding and knowledge of various health topics, as well as share personal opinions and experiences. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this website.

References

Ahlin, A., Bejerkenstedt, L., Fernell, E., … (2011). Altered tryptophan and alanine transport in fibroblasts from boys with attention-deficit/hyperactivity disorder (ADHD): an in vitro study. Retrieved from https://behavioralandbrainfunctions.biomedcentral.com/articles/10.1186/1744-9081-7-40

Banjeree, E. and Nandagopal, K. (2015). Does serotonin deficit mediate susceptibility to ADHD? Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25684070

National Institute on Drug Abuse. (2018). Prescription Stimulants. Retrieved from https://www.drugabuse.gov/publications/drugfacts/prescription-stimulants

U.S. Food and Drug Administration. (2017). Dealing with ADHD: What You Need to Know. Retrieved from https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm269188.htm

WebMD. (2018). ADHD and Substance Abuse. Retrieved from https://www.webmd.com/add-adhd/adhd-and-substance-abuse-is-there-a-link#1

Long Term Effects of ADHD Stimulant Medications

There is consensus in the medical community that the long term brain effects of the medications now being used to treat ADHD is not well documented or well understood. Considering the fact that as of 2016, 6.1 million children and adolescents were diagnosed with ADHD and about 62% receive medication for it, I would say we have a major public health issue. There are some non-stimulants that are being prescribed as well (which we know even less about), but for here we will be focusing on the more commonly prescribed stimulants.

Ritalin was approved by the FDA in the 1950s for treatment of “hyperactivity” but was not really prescribed frequently until the 1960s. It was not being prescribed to children regularly until 1991, when it really seemed to explode. Adderall was not approved by the FDA until 1996. One other consideration is the criteria that was required for approval of these drugs. In my opinion, the requirements for approval were not thorough enough, and sample sizes were not large enough considering the fact that millions of children, adolescents, and adults are now using these drugs. Bourgeois, Mandi, & Kim, 2014 state:

  • There were a total of 32 clinical trials done for the approval of 20 different drugs with each averaging only 75 study participants (Bourgeois et al., 2014).
  • Eleven of the drugs were approved after less than 100 participants were studied
  • Fourteen drugs were approved after less than 300 participants were studied
  • The median trial length prior to FDA drug approval was 4 weeks with five of the approved drugs studied for even less time than that.
  • Six drugs were approved with requests to provide additional data on safety, effectiveness, and optimal usage after the drug was put on the market, called a post-marketing trial. Only two out of the six provided post-marketing trial data.
  • Them minimum age for most trials was 6 years old (only 3 drug studies had a minimum age of 3 years old — Adderall, Biphetamine, and Dexedrine).
  • Only 5 studies out of the 32 (representing 3 drugs) were done to study the safety.
  • Only 8 out of the 32 have been published in medical literature (which would put them under the scrutiny of other doctors/scientists).

“Clinical trials conducted for the approval of many ADHD drugs have not been designed to assess rare adverse events or long-term safety and efficacy.” – Bourgeois, Mandi, & Kim, 2014

For more disappointing information about how these drugs got onto the market, I encourage you to read this study.

Now that we have discussed the prevalence of ADHD, the shocking reality of how these drugs are approved, and the utter lack of long term safety and efficacy data, let’s look at what we are now learning about the long term effects of stimulants.

According to Bottelier et al. (2017), early stimulant medications (treatment started at less than 16 years of age) has long lasting effects on the human brain and behavior, possibly indicating fundamental changes in the dopamine system. These effects are only fully expressed when the system reaches maturation (when the person reaches adulthood) (Bottelier et al., 2017). The dopamine system as well as the GABA neurotransmitter system are still developing during childhood and adolescence. Another study by Luccasen et al (2017) demonstrates that early stimulant exposure lowers baseline GABA neurotransmitter levels in adulthood. Similar to the study by Bottelier et al., the effects on the GABA system are only seen with the full maturation of adulthood.

Should Teachers Be Recommending Evaluations?

“In more than one-half of ADHD cases, it is the educator who requests that a child be assessed for ADHD.” – Ford-Jones, Paediatrics & Child Health Journal, 2015

Even I was surprised when I learned that ADHD medications are known to cause psychotic symptoms in children such as hallucinations, delusions, confused or disturbed thoughts, and lack of self-awareness. I wonder how many teachers have a real understanding of these drugs when they make a suggestion to parents or school psychologists that a child should be evaluated for ADHD. Elementary school teachers usually don’t have any medical background. Schools do not require staff to be educated on ADHD vs appropriate age maturity and behavior, the history of ADHD medications, potential adverse medication side effects and events, and the negative long term effects on neurological function.

What they do know is that once those children are on medication they are easier to handle, they pay attention, they sit down when asked, grades and test scores improve; and when test scores improve, so does school funding. I am not trying to villainize teachers here. I am merely pointing out that educators need to be educated. If teachers are allowed to recommend evaluation, shouldn’t they know a bit about the history of these drugs, and how the drugs may affect the child’s brain development long term? Don’t you think they should be able to ask parents what they do when they get home from school? More sitting, perhaps? Too much screen time? High carbohydrate diet? If a teacher can recommend evaluation for ADHD, should they be able to recommend evaluation by a nutritionist for childhood obesity? Childhood obesity leads to far more dangers than ADHD (although I don’t think obesity harms test scores). 56

There is significant concern for overdiagnosis followed by unnecessarily medicating children, and about 20% of the children that take medication for ADHD are misdiagnosed (Elder, 2010; Ford-Jones, 2015).

If educators were educated on all of these factors we have discussed, maybe they would think twice before recommending evaluation for a “hyperactive” child. My hope is that educating the educators would lead to a significant drop in the ADHD diagnosis rate.

If you have any questions or comments, or if you feel it is necessary to correct something that you read here, feel free to do so below. I appreciate any and all of your contributions. If you think this post could help a friend, share it. You just might change their life.

Related articles that I am working on and will post at a later date:

Top 6 ADHD Triggers To Nix: Stop Giving THESE to Your Child

L-Tryptophan for ADHD: Amino Acids Reduce Symptoms

8 Amino Acids for ADHD

Top 10 Natural Therapies for ADHD (Subscribe to be notified of this post and others)

Cannabidiol (CBD Oil) for ADHD (Subscribe to be notified of this post and others)

Legal Disclaimer: The information, including but not limited to, text, graphics, images, website links and other material contained on this website are for informational purposes only. The purpose of this website is to promote broad consumer understanding and knowledge of various health topics, as well as share personal opinions and experiences. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified healthcare provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this website.

References

Bottelier, M., Bouziane, C., Bron, E., Klein, S., Kooij, J., Reneman, L., & Rombouts, S. (2017). Long-term effects of stimulant exposure on cerebral blood flow response to methylphenidate and behavior in attention-deficit hyperactivity disorder. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5880865/

Bourgeois, F., Mandi, K., & Kim, J. (2014). Premarket Safety and Efficacy Studies for ADHD Medications in Children. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090185/

Centers for Disease Control and Prevention. (2018). Retrieved from https://www.cdc.gov/ncbddd/adhd/features/national-prevalence-adhd-and-treatment.html

Elder, T. (2010). The importance of relative standards in ADHD diagnoses: Evidence based on exact birth dates. Retrieved from https://msu.edu/~telder/2010-JHE.pdf

Ford-Jones, P. (2015). Misdiagnosis of attention deficit hyperactivity disorder: ‘Normal behaviour’ and relative maturity. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443828/

Lucassen, P., Puts, N., Schrantee, A., Solleveld, M., & Reneman, L. (2017). Age-dependent, lasting effects of methylphenidate on the GABAergic system of ADHD patients. Retrieved from https://www.sciencedirect.com/science/article/pii/S2213158217301365